ArticleNeuropathology and applied neurobiology2023
Cytoplasmic HDAC4 recovers synaptic function in the 3×Tg mouse model of Alzheimer's disease.
Article in Neuropathology and applied neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Simvastatin rescues cognitive impairment in an AβNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Gut microbiota as a modulator of HDAC: insights into Alzheimer's disease treatment.Pharmacological reports : PR · 2026Review
- The ketogenic diet alleviates neuronal ferroptosis in epilepsy via HDAC4/TFRC signalling.Archives of medical science : AMS · 2026Article
- N-terminal oligomerization drives HDAC4 nuclear condensation and neurodevelopmental dysfunction inOpen biology · 2025Article
- Review
- Histone Deacetylation in Alzheimer's Diseases (AD); Hope or Hype.Cell biochemistry and biophysics · 2025Review
- SUMOylation balance: a key determinant in synapse physiology.Frontiers in physiology · 2025Review
- A bibliometric analysis of the relationship between traumatic brain injury and Alzheimer's disease (1993-2023).Frontiers in aging neuroscience · 2024Article
- Differential Epigenetic Changes in the Dorsal Hippocampus of Male and Female SAMP8 Mice: A Preliminary Study.International journal of molecular sciences · 2023Article
- Interleukin 1β triggers synaptic and memory deficits in Herpes simplex virus type-1-infected mice by downregulating the expression of synaptic plasticity-related genes via the epigenetic MeCP2/HDAC4 complex.Cellular and molecular life sciences : CMLS · 2023Article
- Exploring the Genetic Predisposition to Epigenetic Changes in Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Cytoplasmic HDAC4 recovers synaptic function in the 3×Tg mouse model of Alzheimer's disease.Neuropathology and applied neurobiology · 2023Article
- SGK1-HDAC4-HMGB1 signaling pathway in the spinal cord dorsal horn participates in diabetic neuropathic pain.Molecular painArticle
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsEarly dysfunction in Alzheimer's disease (AD) is characterised by alterations of synapse structure and function leading to dysmorphic neurites, decreased spine density, impaired synaptic plasticity and cognitive deficits. The class II member HDAC4, which recently emerged as a crucial factor in shaping synaptic plasticity and memory, was found to be altered in AD. We investigated how the modulation of HDAC4 may contribute to counteracting AD pathogenesis.
methodsUsing a cytoplasmic HDAC4 mutant (HDAC4
resultsHere, we report that in wild-type mice, HDAC4 is localised at synapses and interacts with postsynaptic proteins, whereas in the 3×Tg-AD, it undergoes nuclear import, reducing its interaction with synaptic proteins. Of note, HDAC4 delocalisation was induced by both amyloid-β and tau accumulation. Overexpression of the HDAC4
conclusionsThese results highlight a new role of cytoplasmic HDAC4 in providing a structural and enzymatic regulation of postsynaptic proteins. Our findings suggest that controlling HDAC4 localisation may represent a promising strategy to rescue synaptic function in AD, potentially leading to memory improvement.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.